Down-regulation of receptor-activited Smads in seborrheic keratosis

杨扬; 何威; 李颖; 何云志; 黄海; 林自华; 吴军; 杨进清

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Down-regulation of receptor-activited Smads in seborrheic keratosis

更新时间：2026-01-09

- Down-regulation of receptor-activited Smads in seborrheic keratosis
- Journal of Army Medical University Vol. 29, Issue 23, Pages: 2219-2222(2007)
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  CLC： R329-33;R730.23;R739.5
- Published：2007
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杨扬,何威,李颖,何云志,黄海,林自华,吴军,杨进清.脂溢性角化病皮损区受体活化Smad的变化[J].陆军军医大学学报(原第三军医大学学报),2007,29(23):2219-2222.

　YANG Yang,HE Wei,LI Ying,HE Yun-zhi,HUANG Hai,LIN Zi-hua,WU Jun,YANG Jin-qing.Down-regulation of receptor-activited Smads in seborrheic keratosis[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(23):2219-2222.
杨扬,何威,李颖,何云志,黄海,林自华,吴军,杨进清.脂溢性角化病皮损区受体活化Smad的变化[J].陆军军医大学学报(原第三军医大学学报),2007,29(23):2219-2222. DOI：

　YANG Yang,HE Wei,LI Ying,HE Yun-zhi,HUANG Hai,LIN Zi-hua,WU Jun,YANG Jin-qing.Down-regulation of receptor-activited Smads in seborrheic keratosis[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(23):2219-2222. DOI：

摘要

目的探讨转化生长因子β（transforming growth factor-β

TGF-β）信号转导通路中受体活化Smads(Smad2

Smad3)在脂溢性角化病皮损区的表达及其意义。方法采用反转录-实时定量聚合酶链式反应（RT and quantitative Real-Time PCR）和免疫组化技术分别检测脂溢性角化病皮损和正常对照皮肤中Smad2及Smad3的mRNA和Smad1/2/3及磷酸化Smad2/3(p-Smad2/3)蛋白的表达情况。结果与正常对照皮肤组相比，脂溢性角化病皮损中Smad2、Smad3 的mRNA以及Smad1/2/3、p-Smad2/3的表达水平下降。结论脂溢性角化病中受体活化Smads(Smad2、Smad3)和p-Smad2/3表达下调可阻断TGF-β信号转导，可能使TGF-β抑制上皮增生的作用不能有效发挥，从而促进了脂溢性角化病表皮的过度增生。

Abstract

Objective To investigate the expression of receptor-activited Smads (Smad2

Smad3) and phosphorylated Smad2

3 (p-Smad 2/3) in seborrheic keratosis. Methods The skin tissues of seborrheic keratosis from 45 patients (25 males and 20 females

average age: 57.6 years

average course of disease: 3.8 years) who received no treatment before and normal skin tissues from 40 patients (22 males and 18 females

average age: 48 years) undergoing plastic surgery in our hospital were examined for the mRNA levels of Smad2 and Smad3 by quantitative real-time PCR

and the protein levels of Smad1/2/3 and p-Smad2/3 by immunohistochemistry. Results The mRNA levels of receptor-activited Smads (Smad2

Smad3) and the protein levels of Smad1/2/3

p-Smad2/3 were significantly down-regulated in the skin tissues of seborrheic keratosis in comparison with control tissues. Conclusion Down-regulation of receptor-activited Smads (Smad2

Smad3) and p-Smad2/3 might interfere TGF-β signal transduction pathway and contribute to formation of aberrant hyperplastic epidermis in seborrheic keratosis.

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